Fatty Acid Oxidation: Function, Role & Diseases

Fatty acid oxidation or fat burning has its greatest importance in energy production for numerous processes in the body. It takes place in the mitochondria of almost all cells. Various hormones, physical exertion, and certain components of a balanced diet can boost fat burning.

What is fatty acid oxidation?

Fatty acid oxidation is used to produce energy for numerous processes in the body. It takes place in the mitochondria of virtually all cells. Strictly speaking, fatty acid oxidation is a chemical reaction in which the fatty acid donates one or more electrons. These are accepted by another reaction partner, the electron acceptor (Latin, accipere, to accept). In biochemistry, these metabolic reactions are summarized under the term fat oxidation, which contributes to the provision of energy as b-oxidation, a-oxidation or w-oxidation. These three forms differed with respect to the carbon atom at which the oxidation occurs. The b-oxidation (beta-oxidation) is the most significant, with “beta” indicating that the reactions occur at the third carbon atom of the fatty acid. Fatty acid oxidation is fueled by a number of hormones. Growth hormones, glucagon as an antagonist of insulin and thyroid hormones as well as adrenaline are among them. Furthermore, various substances supplied to the body through a balanced diet promote fat burning. Carnitine facilitates transport into the cells, magnesium is needed for the action of various enzymes, and from the amino acid methionine, together with lysine and in the presence of vitamin C, the body can produce carnitine itself.

Function and task

Fat burning ensures that our body has sufficient energy for the uninterrupted processes of building, breaking down and remodeling. Fat oxidation occurs in the mitochondria of cells. These cell organelles are therefore also described as the power plants of the cells. Fatty acid oxidation takes place in several steps. First, the fatty acid must be activated with the participation of coenzyme A as a key molecule. This activated fatty acid enters the mitochondrion with the participation of various carnitine transferases. Transferases are enzymes that transfer chemical groups. Carnitine plays an important role in this transport. In the fitness sector, carnitine is used as a dietary supplement because muscle cells need it for energy production. Once in the mitochondria, the actual breakdown begins. It is subject to a recurring sequence of reaction steps that ends when the final product acetyl CoA has been formed. Depending on the structure of the fatty acid (number of carbon atoms, even- or odd-numbered, saturated or unsaturated fatty acids), additional steps are necessary. In the case of odd-numbered fatty acids, a product is formed that can only be utilized for energy production after conversion in an additional reaction in the subsequent citrate cycle. Fat oxidation occurs constantly in the body, but to varying degrees. It is determined by the demand for energy and depends on physical activity. As the duration of exercise increases, fat burning is activated. At the beginning of physical activity, various hormones cause increased lipolysis, i.e. a breakdown of fats to fatty acids in muscle and adipose tissue. The fats can come from food and from the body’s own adipose tissue. The hormone adrenaline contributes to increased lipolysis. A diet high in carbohydrates causes insulin levels to rise and in this way decreases fat oxidation. Numerous studies have investigated the factors that lead to increased lipolysis. Particularly in the fitness industry and for weight loss programs, key figures such as Fatmax (maximum fat burning rate) are consulted and special tests are developed to determine them. Besides the training condition, the load intensity and the duration influence the fat metabolism rate. Wide individual variations make it difficult to predict which type of physical activity will result in maximum fat burning for each individual.

Diseases and medical conditions

Impaired fatty acid oxidation is most commonly found in people who are overweight. The pancreatic hormone insulin contributes to this by stimulating fat cells to store fat and inhibiting fat burning.Overweight people with very high insulin concentrations therefore find it particularly difficult to reduce weight through fat loss. In addition, there are congenital disorders in fatty acid oxidation. Important enzymes for the transport and conversion of fatty acids are missing or insufficient. As a result, degradation and thus energy production is disturbed. In addition, unconverted intermediates accumulate, triggering toxic reactions in the muscles, brain and liver. One group of disorders affects carnitine metabolism. If too little carnitine is available in the kidneys and muscles, fewer fatty acids are absorbed into the cells of these organs. At preschool age, affected children show muscle weakness and a dysfunctional heart (cardiac insufficiency). The situation worsens particularly dramatically during fasting or after diarrhea. These disorders are treated with the administration of carnitine, often as an injection. If the transporting transferase (carnitine palmitoyl transferase 1 deficiency) is affected, the children show liver and brain damage at an early age. Another disorder affects another type, carnitine palmitoyl transferase 2. The effects of this deficiency show up in adolescence or adulthood as muscle weakness after stress, infections, and food breaks. A low-fat, high-carbohydrate diet and additional administration of triglycerides improve the condition. If the mitochondrial reaction is affected as the actual beta-oxidation, this may be caused by a defect in the dehydrogenase enzyme. If medium-chain acyl-CoA dehydrogenase (MCAD deficiency) is not present in sufficient amounts, life-threatening situations will result if left untreated. The absence of the dehydrogenases that convert very long-chain fatty acids (VLCAD deficiency) leads to damage that affects the heart and results in a drop in blood glucose concentration. As therapy, patients with both forms of dehydrogenase deficiency receive large amounts of carbohydrate and a mixture of medium-length or longer fatty acids adapted to the appropriate causes of disease.